2022 Fiscal Year Research-status Report
Offer insight the mechanism of hepatitis B virus elimination by a novel regulated cell death type: ferroptosis.
Project/Area Number |
22K16033
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Research Institution | National Institute of Infectious Diseases |
Principal Investigator |
闕 路晟 国立感染症研究所, ウイルス第二部, 研究員 (20941636)
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Project Period (FY) |
2022-04-01 – 2025-03-31
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Keywords | HBV / Ferroptosis |
Outline of Annual Research Achievements |
The Hepatitis B virus is a causative agent of Chronic hepatitis B, liver cirrhosis, and hepatocellular carcinoma. Current antiviral drugs interfering viral life cycle, have failed to eradicate infected cells, and the strategies to selectively eliminate infected cells have been awaited. Focusing on a novel type of cell death, the mechanism of how HBV and host immune response sensitize the infected cells to ferroptosis will be investigated.
This year, we found a couple of anti/pro-ferroptotic genes expression is differentially expressed between no-HBV&HBV&HBV+anti-viral drug-treated in a dry/wet analysis; When a human hepatocyte cell line HepG2-NTCP was infected with HBV, a ferroptosis agonist and antagonist decreased and increased HBV infection by in-vitro experiment, respectively;
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Current Status of Research Progress |
Current Status of Research Progress
2: Research has progressed on the whole more than it was originally planned.
Reason
We can spend more time in the laboratory to carry forward this project this year compared with one year ago during the SARS-CoV-2 pandemic.
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Strategy for Future Research Activity |
We have currently identified a couple of anti/pro-ferroptotic genes which involved in HBV infection. In the next year, we try to clarify the role of those genes in HBV infection by performing a lost/gain of function approach. The effect of these genes on viral markers and cell viability will be quantified.
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Research Products
(4 results)